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ENVIRONMENTAL TOBACCO BXO~z A COMPENDIUM OF TECHNICAL INTO~TZON May 1991 DRAFT Q /// This document is a preliminary draft. DO not cite or quote. The contents represent only those views of the individual chapter authors. It should not be construed as representing the views or policies of the participating organizations. /

Draft - Do not cite or quote This compendium of technical perspectives on Environmental Tobacco Smoke (ETS) is intended to be a useful resource document for a diverse audience, including: decislon-makers such as labor and management officials concerned with workplace exposures, public health officials and corporate medical directors who are concerned with making health policy reco~mendations, educators, industrial hygienists and safety officers, ETS researchers, indoor air pollution investigators, and legislators who are considering legislation to restrict smoking in workplaces, restaurants, and public access buildings. Although the technical level varies, even the more technical treatments do not require a specialist's knowledge for understanding. There are eleven chapters in this compilation, including health effects of active smoking in adults a~d passive smoking in children and adults, ETS exposure and dosimetry, comfort aspects, ventilation and ETS, public beliefs about the harm of ETS and attitudes toward controlsr and effective workplace smoking policies, each of which is aimed at a somewhat different audience. Although not all chapters will appeal equally to such a varied group, it is hoped that the technical information in this document, written by experts in the field, will provide information necessary to allow the public, corporations, government agencies, and legislators to make well-lnformed choices regarding exposure to ETS. This perspective on ETS reflects the viewpoints and expertise of authors who were selected based upon their publications and recognition as experts on various aspects of ETS. Accordingly, the opinions expressed do not necessarily represent the official policies of the sponsoring agencies. This document is the result of a coordinated effort jointly sponsored and produced by the Environmental Protection Agency (EPA) (chapters 2,3,4,6,7, and 8), the National Cancer Institute (NCI) (chapters 1,5), the Office on Smoking and Health (centers for Disease Control) (chapter 9), the National Heart, Lung, and Blood Institute (chapter i0), and the office of Disease Prevention and Health Promotion (Department of Health and Human Services) (chapter Ii). The editors acknowledge with gratitude the following distinguished scientists, physicians, and others who lent their support to the development of this document by contributing critical reviews of the various manuscripts, by coordinating manuscript preparation, or assisting in other ways. Mr. Robert Axelrad, H.S. Environmental Protection Agency, 2

Draf~ - Do no~ cite or quote Washington, DC (Sponsor) Dr. Lois Biener, Miriam Hospital, Brown University, Providence, RI Ronald Davis, M.D. Office on Smoking & Health, Centers for Disease Control, Rcckville, MD (Sponsor) James W. Davis, M.D., Veterans' Administration Hospital, Kansas City, MO MS. Hildy Dillon, American Lung Association, New York, NY Dr. Cedric Garland, Dept. of Community Medicine, University of California, San Diego, CA Dr. Stanton A. Glantz, Department of Cardiology, University of California Medical School, San Franscisco, CA Dr. Lawrence Garfinkel, American cancer Society, New York, NY Dr. Katherine Hammond, Dept. of Family & Community Medicine University of Massachusetts Medical Center, Worcester, M-A Dr. Marvin Rristein, State University of New York, Stony Brook, NY State Univ. of New York, Stony Brook Dr. Joellen Lewtas, Office of Research & Development, U.S. Environmental Protection Agency, Research Triangle Park, NC Dr. Alfred H. Lowrey, Laboratory for the Structure of Matter, Naval Research Laboratory, Washington, DC Henry HcIntosh, M.D., A~erican College of Cardiology, Washington, DC Dr. Michael McGinnis, Office of Disease Prevention and Health Promotion, Public Health SerVice, Washington, DC (sponsor) Matthew Meyer, Esq., Coalition on Smoking or Health, Washington, DC D~. Gregory Morosco, Health Education Branch, National Heart, Lung, and Blood Institute, Bethesda, MD (Sponsor) Dr. Demetrios Moschandreas, Illinois Institute of Technology Research Ynstitute, Chicago, IL Dr. David Mudarri, U.S° Environmental Protection Agency, Washington, DC Dr. Terry Pechacek, Smeking, Tobacco, and Cancer Program, National Cancer Institute, Bethesda, MD (Sponsor)

Draft - Do not ¢itm or quota Mr. James Hepace, U.S. Environmental Protection Agency, Washington, DC (Editor) Mr. Donald Shcpland, National Cancer Institute, Bethesda, MD (Editor) John Slade, M.D., Dept, of Medicine, St. Peter's Medical Center, Rutgers University, New Brunswick, NJ Dimitri Trichopoulos, M.D., DrPN, HarVard School of Public Health, Bostcnl HA The editors also acknowledge the comments of the tobacco industry. Mr. Samuel D. Chilcote, Jr., President~ The Tobacco Institute, Washington, DC Dr. Thomas Borelli, Phillip Morris USA, Richmond VA

Draft - Do not cite or quote TABLR OF CONTENTS Chapter I. Effects of Smoking on Smokers. Donald Shopland .............................................. 9 Chapter 2. Environmental Concentrations of ETS. Jo~ McCarthy, Elizabeth Miesner, and John D. Spengler ..................................................... 16 Chapter 3. Measuring Exposure to Environmental Tobacco Smoke. Brian P. Leaderer ............................ ~ ............. 31 Chapter 4. Absorption of Smoke constituents hy Nonsmokers. Dietrich Hoffmann, Klaus D. Brunnemann, and Nancy J. Haley ........................................... 43 Chapter 5. Environmental Tobacco Smoke and Cancer. Jonathan M. Samet ........................................... 67 Chapter 6. Passive Smoking and Heart Disease. S~anton A. Glantz and William W. Parmley ..................... 81 Chapter 7. Exposure Assessment in Passive Smoking. James L. Repace ........................................... 112 Chapter 8. The Odor and Irritation of Environmental Tobacco Smoke. William S. cain ................... • ......................... 137 Chapter 9. Passive Smoking -- Eeliefs, Attitudes, and EXpOsures in the United States. Thomas E. Novotny ........................................... 152 Chapter I0. Passive Smoking and Daycare. Glen L. Bennett ............. ~ .............................. 180 Chapter Ii. NO Smoking Policies at the Worksite: A look at what companies are doing today. Ruth Behrens ............................................... 19T Chapter ii Appendix: Economic Justification for Worksite Smoking Policies. Ruth Behrens ............................................... 219 5

Draft - Do not cite or quote INTRODUCTZON In 1986, the Surgeon General and the National Research Council, the latter under contrac~ to EPA, examined the health effects of the breathing of Environmental Tobacco Smoke (ETS) by nonsmokers (also known as involuntary or passive smoking). They agreed that passive smoking caused lung cancer in ncnsmoking adults, caused increased rates of respiratory infections in children, caused acute noxious effects in many nonsmokers, and was a major contributor to indoor air pollution. Subsequent to the publication of these documents, smoking restrictions began to proliferate. However, a number of diverse technical questions arose concerning public attitudes toward smoking restrictions, health and comfor~ effects, factors affecting exposure, measuring environmental concentrations of ETS, effects of ventilation on ETS and indoor air quality, nonsmokers' u~take of tobacco combustion products, and corporate experience in effective smoking policy, all comprise chapters in this compendium. ~n the interest cf providing answers to this complex of questions, this technical compendium was commissioned. A brief summary of each chapter follows. Chapter 1 demonstrates that high dose exposures to tobacco smoke, i.e., the effects of smoking on smokers, are very toxic, causing cancers, cardiovascular diseases, and respiratory diseases. It is graphically illustrated why cigarette smoking is now recognized as the Nation's. single largest cause of premature death and disability. Chapter 2 reviews studies of the concentrations of certain ETS constituents observed in homes, offices, and other locations by personal exposure monitors. It is concluded that £TS is the primary contaminant contributing to respirable particulate air pollution, and contributes substantially to other indoor contamininants such as benzene, carbon monoxide, and others. Even in low doses, tobacco s~oke contains a wide variety of toxins, including many carcinogens. Chapter 3 treats the methods of assessing nonsmoker's exposure to environmental tobacco smoke by atmospheric markers, and the measurement of these marker substances in indoor air. It is concluded that atmospheric monitoring for respirable particles or nicotine from ETS is critical for assessing exposures and control efforts, and that a number of reliable methods are available for such monitoring. chapter 4 provides a detailed treatment of the absorption and metabolism of tobacco combustion products by nonsmokers. It shows that absorption has been conclusively demonstrated by studies of nicotine and its metabolite, cotinine, in the body fuids of nonsmokers, and that such biomarkers represent a reliable specific method for assaying the level of uptake of ETS. This exemplifies

Draft - Do not cite or quote that low dome exposure to tobacco smoke leads to the absorption of toxins from the smoke in amounts sufficient to potentially cause disease. Chapter B discusses the evidence that low dose exposure to tobacco smoke has been observed to increase the risk of lung cancer i~ nonsmokers, and discusses conclusions of the World Health Organization, the National Research Council, and the U.S. Surgeon General that ETS exposure increases lung cancer incidence in ~cnsmokers. Chapter 6 discusses the evidmnce that low dose exposure to tobacco smoke has been observed to increase the risk of hearu diseases in nonsmokers, and discusses the epidemiological, biochemical, and biological bases for this inference. It is concluded that the combined epidemiological and physlological evidence suggests that ETS exposure is a cause of heart disease in nonsmokers. Chapter 7 investigates the assessment of nonsmokers' exposures tc ETS by mathematical modeling, atmospheric indicators, and % blomarkers in body fluids. Exposures assessed by these various methods produce consistent results. Because of the large source strengtm of tobacco-burning products, exposure to environmental tobacco smoke is inadequately controlled by measures short cf physical separation of smokers and nonsmokers on different ventilation systems, making ETS a significant indoor pollutant of buildings. Chapter 8 explores the effects of ventilation on the perception of odor and irritation from ETS in both nonsmokers and smokers, and shows that attempts to control the odor and irritation of ETS through ventilation and air cleaning have significant limitations. Chapter 9 shows through national surveys of trends in public attitudes, that the general public, including both smokers and nonsmokers, believe that tobacco smoke polluted air is harmful and a large majority find it irritating. There is widespread support for restrictions against smoking, particularly in the workplace. Chapter IC discusses the evidence that smoking both at home and in daycare centers harms children and infants from tobacco- smoke polluted air. This has direct implications for public education of both parents and daycare providers, as well as for state policies and regulations affecting facilities which offer daycare. Chapter II points out the COrydon solution to the problem of ETS ls source control, and examines features of corporate smoking policies in the workplace, with attention to benefits, incentives, employee and union involvement, and education. Case histories are

Draft - Do n¢~ cite or quote ! discussed inv:iving several major corporations, detailing problems encountered and successes. It ks concluded that smoke free workplaces have been achieved in a variety of se~tings. If thoughtfully implemented, they enjoy widespread support.

Draft - Do not cite or quote CHAPTZR 1 BYYECTB OF SMOKING ON SMOKERB Donald 8hopland coordinator Smoking and Tobacco Control Program National cancer ~nstitutes Bethesda, MD Cigarette smoking is the nationts leading cause of premature death and disability. In 1988, smoking caused approximately 390,000 deaths in the United States (Figure i). By 1991, this number had increased to 440,000. In addition, tens of millions of people suffer from chronic disabling diseases and conditions caused or aggrevated by smoking. Every medical authority and organization who has objectively examined the evidence linking smoking to early death and disability has reached a similar conclusion. The 8vidence that smoking is a major health threat is staggering: over 50,000 citations from dozens of cultures are in the scientific literature. Smoking causes or is associated with cancers of the lung and bronchus, larynx, lip and oral cavity, bladder, pancreas, kidney, stomach and cervix, coronary artery disease, cerebrovascular disease (stroke), atherosclerotic aortic aneurysm, atherosclerotic peripheral vascular disease, chronic bronchitis, emphysema, low birth weight babies, and unsuccessful pregnancy. This chapter concentrates on the relationship between active smoking and three diseases caused by ETS -- lung cancer, heart disease, and nonmalignant lung disease. While there are qualitative differences between the mainstream smoke inhaled by the smoker and the ETS nonsmokers inhale, both forms of tobacco smoke contain the same carcinogens, irritants, and other toxins. The effects of high doses of smoke on smokers thus provide an indication of what effects low dose exposures of ETS would be expected to have on nonsmokers. This connection is particularly important because the diseases active smoking causes exhibit dose- response relationships, with higher doses producing greater effects. Because no threshold ham been demonstrated for the carcinogenic and other effects of tobacco smoke on the body, the existence of a dose-response relationship suggests that ETS would provide similar, but smaller, dangers than active smoking. Cancer Most estimates in the scientific literature indicate that nearly one-third of all U.S. cancer deaths result from cigarette smoking. Of the approximately 136,000 cancer deaths which occurred in 1985 because of smoking, 106,00D are of the lung (Figure I). Lung cancer alone is responsible for fully one-quarter of all

Draft - Do not cite or quote cancer mortality; were it not for the increasing number of deaths from lung cancer produced by smoking, we would be experiencing a substantial decline in the cancer death rate in the United StBtes. Approximately 85 to 90 percent of all lung cancer deaths are smoking related. The evidence linking smcking and excess cancer moz~ality is so strong that only the tobacco lobby continues to claim that no causative role has been established. An examination of the association between cigarette smoking and lung cancer graphically illustrates smokingls role in ~he causation of neoplastic diseases. Tobacco smoke contains at least 43 }~no~nn or suspected human carcinogens (Table !), several of which are regulated by the federal government as environmental toxins. There is no known threshold for the carcinogenic effects of these agents. A host of epidemiological studies published during the last two decades provides an abundance of data which demonstrate that exposure to these carcinogens because of smoking leads to an increase in cancer deaths. In particular are the major prospective studies on smoking and health. These studies, conducted in the United States, Canada, England, Japan and Sweden represent some of the largest population based studies ever undertaken by medical science (Table 2). They involved enrolling healthy men and women into a study design and then followed these individual over time. Numerous factor about them were recorded including where they lived, their occupations, dietary habits, whether they used tobacco, access to health care, and many other factors. As a group, these eight studies in the United States, the U.S. Veteran's Study and the American Cancer Society (ACS) 2S-state Study contained cohorts of iS0,000 and I million persons respectively. The Veteran's Study continues to this day and this cohort has been followed prospectively for 26 years. These studies convincingly demonstrate that smoking causes cancer. Lung Cancer Lung canceE mortality rates are strongly influenced by the total dose of cigarette smoke received. If one smokes ~ore cigarettes per day, inhales deeply, if they started smoking at an early age had has smoked for many years, the risk for lung cancer .is increased dramatically. The most often used measure to gauge lung cancer mortality is the number of cigarettes consumed daily. In the ACS 2S-state study, for example, among males smoking less than 1/2 pack per day their lung cancer rate was nearly 5 times greater than that of a nonsmoker. With each increase ix the number of cigarettes consumed daily, a corresponding increase in lung cancer mortality is observed (Figure 2), For those smokers consuming two or more packs daily, their lung cancer mortality is about 24 times greater than i0